Stanford University School of Medicine researchers invented a new algorithm, Baxter Algorithm, to track adult stem cell development more accurately. The main idea was to overcome the difficulties in treating muscle related problems that eventually lead to aging.

According to the research, growing stem cells in the muscle, especially on the developed synthetic matrix, try to copy the elasticity of real muscle, thereby allowing them to retain their auto-renewing agents. Adult stem cells are already present in our body. They play a significant role in forming body tissues in muscles, blood and neurons. So far scientists struggled to create the stem cells in adequate quantity, needed for cell differentiation. Moreover, the stem cells lose some of their qualities immediately after they are kept in a culture dish. One of the qualities is self-renewal. It’s the ability to turn into another stem cell and at the same time the differentiating daughter cell.

This new technique would not only overcome the issue, but it would also help in revolutionizing the application of stem cells in different procedures.  Helen Blau, a researcher at the Stanford’s Institute for Stem Cell Biology and Regenerative Medicine explained, “Cells don’t normally exist in contact with a rigid cell culture dish. They sit on soft tissue. By mimicking this environment we can really influence their function and allow them to self-renew in ways we’ve never been able to achieve before.”

The researchers have developed a new culture system in order to create a more comfortable and softer environment for the stem cells to grow. They used a material, called hydrogel, made of a platform of polyethylene glycol polymers with water. Once they decreased the quantity of polymer molecules, it was turned into a more flexible and more elastic surface.

The researchers let the stem cells grow in the hydrogel for a week. After a week, they found that the softer cells had more cells compared to the less-elastic gels. The scientists had then used the new algorithm to track the cell development automatically. They have found that the cells are not dividing faster. Rather more cells remain alive in the culture dish.

Blau said, “This in itself is a huge advance. Until now it’s been pretty impossible to do these studies without spending half a year or more manually scoring pictures or movies of cells in culture. Now we can figure out exactly how the cells divide and move, who begets who. As a result, we can begin to study all types of variables,” she added, “Clearly the cells grown on the more-elastic surfaces have better survival and self-renewing properties than those grown on standard tissue culture dishes. We conducted our experiments with muscle stem cells, but I expect this will be true for other types of adult stem cells as well.”

Apart from the new algorithm, the researchers continue their work to find out how this advancement would help in stem cells therapies to treat muscle-related problems like muscular dystrophy. Blau said, “Researchers really had no way to grow these cells in the laboratory before. These findings may allow us one day to replenish the muscles of patients with muscular dystrophy and other muscle-wasting diseases with healthy stem cells.”

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Comeback stories are inspiring. They give us hope for the future. This story is about Dream Alliance, a horse whose comeback story to recover from Achilles tendon injuries will offer hope for many. Wondering why this is a big story? Read on.

The Achilles tendon is the largest tendon in our body that connects the calf muscle with the heel bone. The Achilles tendon goes through a lot when we run or jump or lead an active life. This is the reason that many athletes and players suffer from Achilles tendon injuries. However what makes it worse is, almost 25 to 45% of these injuries need surgery and the patients’ lives largely depend on the crutches.

Dream Alliance went through an Achilles tendon injury while running in a race in 2008. He cut a tendon in the front leg. His condition was so critical that he was almost considered to be euthanized. But a stem cell treatment helped him recover from his injury and at the same time get back on his career. The process was very simple. Bone marrow was collected from the hip of the horse and mesenchymal stem cells were isolated. The mesenchymal stem cells were moved to a petri dish in order to create millions of cells. Once the required amount of cells were produced, they were injected into the affected tendon directly.

The procedure conducted by the researchers at the University College of London and the Royal National Orthopaedic Hospital proved successful for the horses. Now the team is conducting a stem cell clinical trial to treat Achilles tendon injuries in humans. Andrew Goldberg, the team lead of the study explained, “Tendon injuries in horses are identical to those in humans, and using this evidence from the 1500 treated horses] we were able to persuade the regulators to allow us to launch a small safety study in humans.”

So far the trial involving humans is going well and is showing positive results. One of the patients, who was suffering from Achilles tendon injury said, “I worried, because no one had ever had it before, except a horse. But I was more worried I’d end up in a wheelchair. The difference now is amazing. I can do five miles on the treadmill without pain, and take my dog Honey on long walks again.” The 46-year old used to lead a very busy life until she started feeling a severe ankle pain, as a result of an Achilles tendon injury.

The team at the University College of London and the Royal National Orthopaedic Hospital is still unsure on how this therapy works to heal the tendon injury; however, they have used the mesenchymal stem cells, which have the regeneration ability. They are also known to reduce inflammation. The first case’s being successful is very motivating. Researchers are hopeful that they will be able to find out a definite cure for Achilles tendon injuries for humans. For an effective result, researchers need a large number of patients, so that they can gather the varied data in one single study.

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Duchenne muscular dystrophy or DMD is a serious genetic disorder that affects hundreds of children every year. This disorder leads to conditions like atrophy and muscle weakness. There is no cure for the disease, however, supportive care can be offered to take care of their lungs and heart but these arrangements can only extend their lives till 27.

Now what causes Duchenne muscular dystrophy so dangerous for children? Kids, suffering from DMD cannot produce dystrophin, a protein that helps to keep away the muscles from breaking. The main reason is, these people have gone through a mutation in their gene in the X chromosome, which is responsible for providing the blueprint for dystrophin. The genetic mutation may lead to a more critical situation where most parts of the dystrophin get affected and a result the body stops producing the protein completely.

For some people with DMD, there are so many errors in the gene that the body cancels out the affected protein the moment it’s created. However, what’s more interesting to see is, the researchers have concentrated on the genes that are completely flawed and that interrupt in reading blueprint to produce dystrophin.

In order to address the criticalness of this condition, researches have conducted a study on a mice model. Multiple groups of researchers have harnessed the technique of applying gene editing enzyme complex CRISPR in order to modify the genes of mice with DMD. The technique allows cutting the errors in the genetic code, so that their effects can simply be avoided. After that the body starts to read the gene and then produce a shorter version of the protein that manages to protect the muscles from breaking down so easily, much like the process to treat patients with Becker muscular dystrophy.

The process involves loading the CRISPR complex into a virus and then injecting it to the mice fetus with DMD. The researchers have found that the mice began to create the shortened protein once the virus is injected into them. This helped the mice to resume the power of their muscles, which gradually led to a concrete treatment of their disease. So, the research was quite successful on the mice model.

The findings have generated a thin window of hope for the people, suffering with Duchenne muscular dystrophy mutation as well. But the process was easier for mice, and the researchers know that it’s not going to be the same easy game for humans. Moreover, no matter how foolproof the technique is proved for the mice, it may not deliver the same results on humans.

The scientists have established that the CRISPR can cut away additions to the gene but it will still take some time to show if it can address other kinds of mutations at all. Researchers are also not sure about the reactions of CRISPR complex in humans. Chances are that they might get rejected by the human immune system altogether. If it does not prove to be a 100% fix to the disorder, it means that the technique will not be able to treat all patients with Duchenne muscular dystrophy mutation.

However, having said all these, it’s also true that this research is the first ever experiment to have shown success, even if on a mice model. And researchers are hopeful that with more clinical trials, they might achieve the desired results soon.

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